MDA-9/Syntenin regulates differentiation and angiogenesis programs in head and neck squamous cell carcinoma

Oyesanya, Regina A.; Menezes, Mitchell E.; Dumur, Catherine I.; Singh, Karan P.; Bae, Sejong; Troyer, Dean A.; Wells, Robert B.; Sauter, Edward R.; Sidransky, David; Fisher, Paul B.; Semmes, O. John; Dasgupta, Santanu

doi:10.18632/oncoscience.99

Cited by 27 publications

(33 citation statements)

References 31 publications

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“…Stable clones were selected in the presence of puromycin (10 mg/mL). A single stable clone was expanded and utilized for all subsequent analyses (14,15).…”

Section: Lentiviral Transduction Of Sh3gl2mentioning

confidence: 99%

“…Stable clones were selected in the presence of puromycin (1 mg/mL). A single stable clone was expanded and utilized for all subsequent analyses (14,15). In both gain and loss-offunction studies, na€ ve control cells were used to examine the influence of the empty vector on SH3GL2 expression.…”

Section: Lentiviral Transduction Of Sh3gl2mentioning

confidence: 99%

“…IHC and immunofluorescence (IF) analyses were performed as described previously (14,15). The IF Images were captured through a Leica TCS SP8 laser-scanning confocal imaging station (Leica Microsystems).…”

Section: Ihc and Immunofluorescencementioning

confidence: 99%

“…14, 15). Soft agar colony formation and invasion assays (#354481, Corning) were performed as described earlier (14,15). In all cases, data were presented as mean AE SE of duplicate experiments.…”

Section: Translational Relevancementioning

confidence: 99%

“…Preparation of whole-cell or mitochondrial lysates, Western blotting analysis, and immunoprecipitation were performed following protocols described earlier (14,15).…”

Section: Western Blotting and Coimmunoprecipitation Analysismentioning

confidence: 99%

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Mitochondrial Reprogramming Regulates Breast Cancer Progression

Kannan

Wells

Sivakumar³

et al. 2016

Clinical Cancer Research

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Purpose: The goal of this study was to understand the role of altered mitochondrial function in breast cancer progression and determine the potential of the molecular alteration signature in developing exosome-based biomarkers.Experimental Design: This study was designed to characterize the critical components regulating mitochondrial function in breast tumorigenesis. Experiments were conducted to assess the potential of these molecules for exosome-based biomarker development.Results: We observed a remarkable reduction in spontaneous metastases through the interplay in mitochondria by SH3GL2, vesicular endocytosis-associated protein and MFN2, an important regulator of mitochondrial fusion. Following its overexpression in breast cancer cells, SH3GL2 translocated to mitochondria and induced the production of superoxide and release of cytochrome C from mitochondria to the cytoplasm. These molecular changes were accompanied by decreased lung and liver metastases and primary tumor growth. SH3GL2 depletion reversed the above phenotypic and associated molecular changes in nontumorigenic and tumorigenic breast epithelial cells. Loss of SH3GL2 and MFN2 expression was evident in primary human breast cancer tissues and their positive lymph nodes, which was associated with disease progression. SH3GL2 and MFN2 expression was detected in sera exosomes of normal healthy women, but barely detectable in the majority of the women with breast cancer exhibiting SH3GL2 and MFN2 loss in their primary tumors.Conclusions: This study identified a new mitochondria reprogramming pathway influencing breast cancer progression through SH3GL2 and MFN2. These proteins were frequently lost in breast cancer, which was traceable in the circulating exosomes. Clin Cancer Res; 22(13); 3348-60. Ó2016 AACR.

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“…Stable clones were selected in the presence of puromycin (10 mg/mL). A single stable clone was expanded and utilized for all subsequent analyses (14,15).…”

Section: Lentiviral Transduction Of Sh3gl2mentioning

confidence: 99%

Section: Lentiviral Transduction Of Sh3gl2mentioning

confidence: 99%

Section: Ihc and Immunofluorescencementioning

confidence: 99%

Section: Translational Relevancementioning

confidence: 99%

“…Preparation of whole-cell or mitochondrial lysates, Western blotting analysis, and immunoprecipitation were performed following protocols described earlier (14,15).…”

Section: Western Blotting and Coimmunoprecipitation Analysismentioning

confidence: 99%

See 3 more Smart Citations

Mitochondrial Reprogramming Regulates Breast Cancer Progression

Kannan

Wells

Sivakumar³

et al. 2016

Clinical Cancer Research

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Complex‐I Alteration and Enhanced Mitochondrial Fusion Are Associated With Prostate Cancer Progression

Philley

Kannan

Qin

et al. 2015

Journal Cellular Physiology

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Mitochondria (mt) encoded respiratory complex-I (RCI) mutations and their pathogenicity remain largely unknown in prostate cancer (PCa). Little is known about the role of mtDNA loss on mt integrity in PCa. We determined mtDNA mutation in human and mice PCa and assessed the impact of mtDNA depletion on mt integrity. We also examined whether the circulating exosomes from PCa patients are transported to mt and carry mtDNA or mt proteins. We have employed next generation sequencing of the whole mt genome in human and Hi-myc PCa. The impact of mtDNA depletion on mt integrity, presence of mtDNA, and protein in sera exosomes was determined. A co-culture of human PCa cells and the circulating exosomes followed by confocal imaging determined co-localization of exosomes and mt. We observed frequent RCI mutations in human and Hi-myc PCa which disrupted corresponding complex protein expression. Depletion of mtDNA in PCa cells influenced mt integrity, increased expression of MFN1, MFN2, PINK1, and decreased expression of MT-TFA. Increased mt fusion and expression of PINK1 and DNM1L were also evident in the Hi-myc tumors. RCI-mtDNA, MFN2, and IMMT proteins were detected in the circulating exosomes of men with benign prostate hyperplasia (BPH) and progressive PCa. Circulating exosomes and mt co-localized in PCa cells. Our study identified new pathogenic RCI mutations in PCa and defined the impact of mtDNA loss on mt integrity. Presence of mtDNA and mt proteins in the circulating exosomes implicated their usefulness for biomarker development.

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